SUMMARY OF WORK. This research investigates physiological mechanisms associated with behavioral factors that potentiate sustained hypertension. Previous studies with humans showed that high perceived chronic stress is associated with slower breathing frequency at rest and higher resting end tidal CO2 (which is an index of pCO2). Voluntary increases in end tidal CO2 during controlled breathing have been shown to transiently decrease plasma pH and renal sodium excretion, and increase plasma and urinary concentration of endogenous digitalis-like factors that inhibit sodium pump activity. Other studies showed that older African Americans, who are known to have delayed renal sodium excretion and greater prevalence of hypertension, have higher resting end tidal CO2 and lower excretion of urinary MBG than older Caucasians, matched for age and gender. Over the past year, data has been collected showing that the rate of 24-hr urinary excretion of one of these factors, marinobufagenin, is lower in healthy humans in the Baltimore Longitudinal Study on Aging with high, as opposed to low, resting end tidal CO2. An association of high resting end tidal CO2 with elevated resting blood pressure has been shown to be most prominent in women who suppress the expression of anger. Over the past year, we have found that characteristic anger suppression is also associated with increased carotid arterial stiffness, independent of age, gender, race and body mass index. This effect was specific to older persons (i.e. over age 58). No such effects are observed in those who characteristically express anger. An experimental study of the effects of high sodium intake on ambulatory blood pressure and 24-hr urinary excretion of endogenous digitalis-like factors in humans with both rapid and slow breathing patterns has been initiated.